Celiac Disease – If You Have ANY of These Symptoms, STOP Eating Gluten Immediately

It turns out that only a small number of people who have genetic predisposition to develop celiac disease actually witness the emergence of this disease.

Science still doesn’t have an answer why is this happening. However, a new scientific study indicates that it is all about the reaction of specific gut bacteria to gluten.

In case you didn’t know, celiac disease is a type of immune disease in which individuals are gluten intolerant. Gluten is a type of protein which can usually be found in grains like barley, wheat and rye. According to some stats about 1% of Americans are dealing with celiac disease.

In case a person suffering from celiac disease eats gluten, their immune system will create a reaction that will cause damage in the small intestine. As a result of this reaction, people usually experience diarrhea, abdominal pain, fatigue, bloating and other similar symptoms. Specific gene mutations can also lead to celiac disease. But, less than 3% of people who have these mutations end up with this health condition.

In order to determine why is this happening, Dr. Elena F. Verdu who works at the McMaster University in Canada together with her fellow scientists, decided to focus on the link between gluten mixed with different types of gut bacteria and immune system’s reactions in lab mice.

The interesting results they got were revealed in the American Journal of Pathology. Mice free of germs displayed signs and symptoms of celiac disease as a response to gluten presence. The group of scientists evaluated the results in three different groups of lab mice that had DQ8 gene which is the same gene found in humans that makes them prone to gluten intolerance.

Things You Should Know About Celiac Disease

More than 80% of Americans dealing with celiac disease are misdiagnosed with other health conditions or are not diagnosed at all.

There is only one treatment for celiac disease recommended by scientists – following a gluten-free diet.

Between 15% and 22% of persons suffering from celiac disease have a close relative with this condition.

So, each of the three groups of mice had different composition of gut bacteria/microbiomes. One of the groups was clear SPF (specific pathogen free) and had gut bacteria compositions that didn’t have proteobacteria. The second group was free of germs and the last group consisted of mice with conventional specific pathogen free individuals. They had a huge range of gut bacteria like proteobacteria and some so-called opportunistic pathogens like streptococcus, staphylococcus and helicobacter.

The scientists gave gluten to all mice. They concluded that the germ-free animals have experienced higher levels of intraepithelial lymphocytes in their gut. It is good to mention that the activation and production of intraepithelial lymphocytes is considered to be an early sign of celiac disease. On the other hand, boosted IEL levels were not noticed in mice with clean SPF.

In addition, the mice that were free of germs had boosted cell deaths in the gastrointestinal tract known as enterocytes together with anatomical modifications of the tiny protrusions that line the small intestine called villi.

This research has also managed to find the progress of antibodies as a reaction to a compound found in gluten known as gliadin in germ-free lab mice and in addition, these lab mice also shown T-cell responses closely related to this compound.

What is even more interesting is that the group of scientists concluded that the development of pathology induced by gluten was stopped in the clean SPF lab mice when compared to the mice that were free of germs. However, the situation was different when clean SPF lab mice got entero-adherent Escherichia coli from a person suffering from celiac disease.

Higher levels of proteobacteria made the pathology induced by gluten worse

Regular SPF mice shown higher gluten-induced pathology compared to clean SPF lab mice and that’s why the team decided to focus their research on the activity and role of proteobacteria varieties like helicobacter and Escherichia.

By making the level of proteobacteria higher in regular SPF lab mice with the help of vancomycin (antibiotic) after their birth, the scientists have concluded that the pathology induced with gluten becomes worse. They have pointed out that the levels of IELs became significantly higher.

Dr. Verdu said that their studies show that deviation of early-stage colonization of microbes in life and dysbosis induction (imbalance related to microbes in the body) that results in increased presence of proteobacteria, increases the harshness of responses triggered by gluten in lab mice that have genetic predisposition to gluten sensitivity.

She also pointed out that the data they got suggests that the noted increase in celiac disease presence in people in the last five decades could be induced (at least to some extent) by divation in intestinal microbial flora. Certain therapies based on microbiota may support the prevention or healing of celiac disease in people with mild to moderate genetic risk.

A review of this study, performed by Dr. Robin Lorenz (University of Alabama, Birmingham), highlights the fact that while it is true that these results support the idea that the level of proteobacteria may be directly related to the celiac disease pathology, it is also true that there is no indication that proteobaceria actually lead to this disease. Dr. Lorenz believes that proteobacteria support the immune response to gluten or to gliadin to be more precise.

A few weeks ago, a scientific study published in the Medical News Today has shown that people suffering from celiac disease may be more prone to nerve damage.